It now seems that adipose hexose transfer is subject to at least two forms of regulation - the well-documented, insulin-induced carrier recruitment from cytosol to plasma membrane and a recruitment-independent mechanism. Here we show that both rat adipose and erythrocyte sugar transport may share a common susceptibility to regulation by this 'recruitment'-independent mechanism. The kinetics of sugar transport in normal rat adipose and erythrocytes are symmetric. Following rat hypophysectomy, however, both adipose and RBC sugar transport become asymmetric - exit rates being greater than those for entry. Under these conditions, insulin accelerates adipose sugar uptake but not exit. The striking parallels between adipose and RBC hexose transfer responses to hypophysectomy have enabled us to exploit the RBC as a model system for the study of this type of transport regulation. The result has been the discovery of 'active principles' in both rat serum and RBC cytosol from hypophysectomized rats that control the expression of red cell sugar transport symmetry, the number of RBC hexose transport proteins and the average molecular weight of the transporter. Our goal is to exploit this endocrinological approach to determine: 1. The origin of increased RBC hexose transfer protein numbers. 2. The molecular basis of RBC transport symmetry expression. 3. The susceptibility of adipose hexose transfer to these transport modulating factors. 4. The effects of these factors on insulin-induced adipose carrier recruitment.